The two hallmark features of fibromyalgia (FM) are that (a) all persons with the disorder exhibit abnormal pain sensitivity; and (b) nearly 90% of persons with FM are women. Current models of the etiopathogenesis of FM suggest there may be a genetic susceptibility to the development of abnormal pain indicates that sex-dependent, familial contributions to pain sensitivity may contribute to abnormal nociceptive transmission or modulation among women with FM. Indeed, one study suggests that women with FM are significantly more likely than healthy controls to exhibit a functional polymorphism in the promoter region of the serotonin transporter gene (5-HTT) that might contribute to altered serotonergic neurotransmission and abnormal pain sensitivity. Therefore, we propose to test 7 hypotheses regarding the extent to which female and male siblings of female FM probands, compared to the female and male siblings of sex-matched, pain-fee controls, differ in (a) pain sensitivity in response to diverse stimuli (i.e., pressure, thermal, ischemic); and (b) blood serum levels of serotonin. We also will compare the FM patient probands and controls on pain sensitivity, serotonin levels, and the presence of the above-noted functional polymorphism among the 4 sibling groups. We anticipate a rank-ordering of pain sensitivity and serum serotonin across the subject groups with the greatest sensitivity and lowest serotonin levels among the FM probands, followed by their female siblings, followed by their male siblings, and then among the controls and their siblings. We also anticipate that group differences in serotonin will partially mediate the group differences in pain sensitivity. We believe our results will increase our understanding of the role of sex- related influences on abnormal pain sensitivity in FM.